The broad, long-term goal of this project is to elucidate the mechanisms by which specific stress proteins reduce oxidative damage, and to develop strategies by which the heat shock family of stress proteins can increase ischemic cardioprotection. One of the specific aims is to establish whether gain of function of specific stress protein expression, under the control of an inducible-system, will rescue ischemic susceptibility of HSF1-deficient mice through effects that ameliorate oxidative stress/damage, enhance cardiac metabolism, and restore ventricular function. We have initiated studies to assess cardiac metabolism and function using (1) both the Langendorff and the work-performing isolated perfusion heart models, and (2) 31P NMR spectra to measure high energy metabolites. (Service 6) REPORT PERIOD: (09/01/97-08/31/98)